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Review
. 2015 May 28;7(9):1258-64.
doi: 10.4254/wjh.v7.i9.1258.

Bone changes in alcoholic liver disease

Affiliations
Review

Bone changes in alcoholic liver disease

Emilio González-Reimers et al. World J Hepatol. .

Abstract

Alcoholism has been associated with growth impairment, osteomalacia, delayed fracture healing, and aseptic necrosis (primarily necrosis of the femoral head), but the main alterations observed in the bones of alcoholic patients are osteoporosis and an increased risk of fractures. Decreased bone mass is a hallmark of osteoporosis, and it may be due either to decreased bone synthesis and/or to increased bone breakdown. Ethanol may affect both mechanisms. It is generally accepted that ethanol decreases bone synthesis, and most authors have reported decreased osteocalcin levels (a "marker" of bone synthesis), but some controversy exists regarding the effect of alcohol on bone breakdown, and, indeed, disparate results have been reported for telopeptide and other biochemical markers of bone resorption. In addition to the direct effect of ethanol, systemic alterations such as malnutrition, malabsorption, liver disease, increased levels of proinflammatory cytokines, alcoholic myopathy and neuropathy, low testosterone levels, and an increased risk of trauma, play contributory roles. The treatment of alcoholic bone disease should be aimed towards increasing bone formation and decreasing bone degradation. In this sense, vitamin D and calcium supplementation, together with biphosphonates are essential, but alcohol abstinence and nutritional improvement are equally important. In this review we study the pathogenesis of bone changes in alcoholic liver disease and discuss potential therapies.

Keywords: Alcoholism; Bone fractures; Liver disease; Osteoporosis; Vitamin D.

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Figures

Figure 1
Figure 1
Factors that contribute to bone disease in alcoholic patients.
Figure 2
Figure 2
Pathogenesis of alcoholic bone disease and potential therapies. Bone disease in alcoholic patients is due basically to decreased bone formation (decreased osteoblast activity and poor mineralization) and increased bone degradation (increased osteoclast activity). Potential therapies should counteract these effects but the mainstay of treatment should be alcohol abstinence. RANK: Receptor activator of nuclear factor kappa-B; RANK-L: RANK ligand; OPG: Osteoprotegerin.

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